@article{causin_rufty_reynolds_2006, title={Gas exchange and carbon metabolism in two Prosopis species (Fabaceae) from semiarid habitats: Effects of elevated CO2, N supply, and N source}, volume={93}, ISSN={["1537-2197"]}, DOI={10.3732/ajb.93.5.716}, abstractNote={Predicting future plant and ecosystem responses to elevated CO(2) also requires an understanding of the role of other factors, especially soil nitrogen. This is particularly challenging for global aridlands where total N and the relative amounts of nitrate and ammonia vary both spatially and seasonally. We measured gas exchange and primary and secondary C metabolites in seedlings of two dominant aridland shrub species (Prosopis flexuosa [S America] and P. glandulosa [N America]) grown at ambient (350 ppm) or elevated (650 ppm) CO(2) and nitrogen at two levels (low [0.8 mM] and high [8.0 mM]) and at either 1 : 1 or 3 : 1 nitrate to ammonia. Whereas elevated CO(2) increased assimilation rate, water use efficiency, and primary carbon metabolites in both species, these increases were strongly contingent upon nitrogen availability. Elevated CO(2) did not increase secondary metabolites (i.e., phenolics). For these important aridland species, the effects of elevated CO(2) are strongly influenced by nitrogen availability and to a lesser extent by the relative amounts of nitrate and ammonia supplied, which underscores the importance of both the amount and chemical composition of soil nitrogen in mediating the potential responses of seedling growth and establishment of aridland plants under future CO(2)-enriched atmospheres.}, number={5}, journal={AMERICAN JOURNAL OF BOTANY}, author={Causin, HF and Rufty, TW and Reynolds, JF}, year={2006}, month={May}, pages={716–723} }
 @article{milla_levin_lewis_rufty_2005, title={RAPD and SCAR markers linked to an introgressed gene conditioning resistance to Peronospora tabacina D.B. Adam in tobacco}, volume={45}, ISSN={["1435-0653"]}, DOI={10.2135/cropsci2004.0754}, abstractNote={Blue mold, caused by the fungal pathogen Peronospora tabacina D.B. Adam, is one of the most important foliar diseases of tobacco ( Nicotiana tabacum L.). Identification of molecular markers linked to genetic factors controlling resistance would facilitate development of resistant cultivars. Bulked segregant analysis was used to screen 1216 random amplified polymorphic DNA (RAPD) primers for their ability to reveal polymorphism between DNA bulks from susceptible doubled haploid (DH) lines and resistant DH lines possessing resistance derived from cultivar Ovens 62. Fifteen RAPD markers were tentatively identified as being linked to a major gene conditioning resistance to blue mold. These 15 markers (12 in coupling phase linkage with resistance and three in repulsion phase) were found to lie within a single linkage group of 36.6 cM and were subsequently tested on 122 DH lines derived from crosses between resistant and susceptible parents. F tests revealed statistically significant associations between resistance and each of the 15 RAPD markers. Interval mapping was used to more accurately place the quantitative trait locus (QTL) controlling resistance on the linkage map. The RAPD markers were screened on a set of 45 resistant and susceptible cultivars or breeding lines and four Nicotiana species. At variance with previous reports, marker genotypes indicated that resistance in Ovens 62 and most other blue mold resistant lines likely originated from N. debneyi Domin. Two RAPD markers flanking the most likely QTL position were converted to sequence characterized amplified region (SCAR) markers. These markers should aid in development of blue mold‐resistant tobacco cultivars worldwide.}, number={6}, journal={Crop Science}, publisher={Crop Science Society of America}, author={Milla, S.R. and Levin, J.S. and Lewis, R.S. and Rufty, R.C.}, year={2005}, pages={2346–2354} }
 @misc{rufty_2005, title={Tobacco cultivar NC 2000}, volume={6,965,062}, publisher={Washington, DC: U.S. Patent and Trademark Office}, author={Rufty, R. C.}, year={2005} }
 @article{johnson_wolff_wernsman_rufty_2002, title={Marker-assisted selection for resistance to black shank disease in tobacco}, volume={86}, ISSN={["1943-7692"]}, DOI={10.1094/PDIS.2002.86.12.1303}, abstractNote={Bulked segregant (BSA) and random amplified polymorphic DNA (RAPD) analyses were used to identify markers linked to the dominant black shank resistance gene, Ph, from flue-cured tobacco (Nicotiana tabacum) cv. Coker 371-Gold. Sixty RAPD markers, 54 in coupling and 6 in repulsion phase linkage to Ph, were identified in a K 326-derived BC1F1 (K 326-BC1F1) doubled haploid (DH) population. Thirty RAPD markers, 26 in coupling and 4 in repulsion phase linkage to Ph, were used to screen 149 K 326-BC2F1 haploid plants. Complete linkage between the 26 coupling phase markers and Ph was confirmed by screening 149 K 326-BC2F1 DH lines produced from the haploid plants in black shank nurseries. RAPD markers OPZ-5770 in coupling and OPZ-7370 in repulsion phase linkage were used to select plants homozygous for the Ph gene for further backcrossing to the widely grown flue-cured cultivar K 326. Black shank disease nursery evaluation of 11 K 326-BC4S1 lines and their testcross hybrids to a susceptible tester confirmed linkage between Ph and OPZ-5770. The results demonstrated the efficiency of marker-assisted selection for Ph using a RAPD marker linked in coupling and repulsion. Complete linkage between 26 RAPD markers and the Ph gene was confirmed in the K 326-BC5 generation, and RAPD phenotypes were stable across generations and ploidy levels. These RAPD markers are useful in marker-assisted selection for Ph, an important black shank resistance gene in tobacco.}, number={12}, journal={PLANT DISEASE}, author={Johnson, ES and Wolff, MF and Wernsman, EA and Rufty, RC}, year={2002}, month={Dec}, pages={1303–1309} }
 @article{herrero_rufty_daub_2001, title={Molecular determinants influencing the inheritance of transgenic virus resistance in segregating tobacco families transformed with the nucleocapsid gene of tomato spotted wilt virus}, volume={7}, ISSN={["1572-9788"]}, DOI={10.1023/A:1011381412397}, number={2}, journal={MOLECULAR BREEDING}, author={Herrero, S and Rufty, RC and Daub, ME}, year={2001}, pages={131–139} }
 @article{herrero_culbreath_csinos_pappu_rufty_daub_2000, title={Nucleocapsid gene-mediated transgenic resistance provides protection against Tomato spotted wilt virus epidemics in the field}, volume={90}, DOI={10.1094/phyto.2000.90.2.139}, abstractNote={ABSTRACT Transformation of plants with the nucleocapsid (N) gene of Tomato spotted wilt tospovirus (TSWV) provides resistance to disease development; however, information is lacking on the response of plants to natural inoculum in the field. Three tobacco cultivars were transformed with the N gene of a dahlia isolate of TSWV (TSWV-D), and plants were evaluated over several generations in the greenhouse. The resistant phenotype was more frequently observed in 'Burley 21' than in 'KY-14' or 'K-326', but highly resistant 'Burley 21' transgenic lines were resistant to only 44% of the heterologous TSWV isolates tested. Advanced generation (R(3) and R(4)) transgenic resistant lines of 'Burley 21' and a 'K-326' F(1) hybrid containing the N genes of two TSWV isolates were evaluated in the field near Tifton, GA, where TSWV is endemic. Disease development was monitored by symptom expression and enzyme-linked immunosorbent assay (ELISA) analysis. Whereas incidence of TSWV infection in 'Burley 21' susceptible controls was 20% in 1996 and 62% in 1997, the mean incidence in transgenic lines was reduced to 4 and 31%, respectively. Three transgenic 'Burley 21' lines were identified that had significantly lower incidence of disease than susceptible controls over the two years of the study. In addition, the rate of disease increase at the onset of the 1997 epidemic was reduced for all the 'Burley 21' transgenic lines compared with the susceptible controls. The 'K-326' F(1) hybrid was as susceptible as the 'K-326' nontransformed control. ELISA analysis demonstrated that symptomless plants from the most resistant 'Burley 21' transgenic lines accumulated detectable nucleocapsid protein, whereas symptomless plants from more susceptible lines did not. We conclude that transgenic resistance to TSWV is effective in reducing incidence of the disease in the field, and that accumulation of transgene protein may be important in broad-spectrum resistance.}, number={2}, journal={Phytopathology}, author={Herrero, S. and Culbreath, A. K. and Csinos, A. S. and Pappu, H. R. and Rufty, R. C. and Daub, M. E.}, year={2000}, pages={139–147} }
 @article{ng'ambi_rufty_barker_1999, title={Genetic analysis of Meloidogyne arenaria race 1 resistance in tobacco}, volume={83}, ISSN={["1943-7692"]}, DOI={10.1094/PDIS.1999.83.9.810}, abstractNote={Inheritance of resistance to the peanut root-knot nematode (Meloidogyne arenaria (Neal) Chitwood race 1) was investigated in the flue-cured tobacco cv. Speight G 28 and the breeding lines 81-RL-2K and SA 1214. The genetic relationship of this resistance in Speight G 28 to the resistance of the same cultivar to races 1 and 3 of M. incognita was also studied. Crosses were made between the root-knot nematode-susceptible flue-cured tobacco cv. NC 2326 and the three resistant genotypes. Parental, F 1 , F 2 and backcross generations (BC 1 P 1 , BC 1 P 2 ) were grown for each cross in randomized complete block designs with five replications in the greenhouse. Data indicated that resistance to M. arenaria race 1 in the three resistance sources is conditioned by a single dominant gene, but this resistance is partial compared to that for M. incognita races 1 and 3. Further, resistance to races 1 and 3 of M. incognita and resistance to M. arenaria race 1 in cv. Speight G 28 appear to be controlled by the same gene. These results, combined with the absence of segregation in the F 2 populations of the crosses between resistant parents 81-RL-2K × SA 1214, 81-RL-2K × Speight G 28, and SA 1214 × Speight G 28, suggest allelism of resistance among these genotypes.}, number={9}, journal={PLANT DISEASE}, author={Ng'ambi, TBS and Rufty, RC and Barker, KR}, year={1999}, month={Sep}, pages={810–813} }
 @article{ng'ambi_rufty_barker_melton_1999, title={Identification of sources of resistance to four species of root-knot nematodes in tobacco}, volume={31}, number={3}, journal={Journal of Nematology}, author={Ng'ambi, T. B. S. and Rufty, R. C. and Barker, K. R. and Melton, T. A.}, year={1999}, pages={272–282} }
 @article{yi_rufty_wernsman_conkling_1998, title={Mapping the root-knot nematode resistance gene (Rk) in tobacco with RAPD markers}, volume={82}, ISSN={["0191-2917"]}, DOI={10.1094/PDIS.1998.82.12.1319}, abstractNote={Random amplified polymorphic DNA (RAPD) analysis was conducted to map the Rk gene in tobacco which conditions resistance to races 1 and 3 of the root-knot nematode, Meloidogyne incognita. Resistant burley tobacco genotype NC 528, containing the Rk gene, and the susceptible cultivar Ky 14 were screened with 1,500 random decamers. A low rate of genetic polymor-phism (<10%) was detected among these lines. Two populations (F 1 and F 3 ) of maternally de-rived doubled haploid (MDH) lines of burley tobacco, developed from the cross NC 528 × Ky 14, were used to map the Rk gene. NC 528, Ky 14, three Rk-resistant (Rk-R) DNA bulks, andthree Rk-susceptible (Rk-S) bulks generated from F 1 -derived MDH individuals were screenedwith the primers that amplified bands polymorphic between Rk-R and Rk-S lines. A total of 67 F1MDH lines and 59 F3MDH lines were screened with the primers that amplified bands polymorphic between Rk-R bulks and Rk-S bulks to confirm linkage between candidate markers and the Rk gene. Sixteen RAPD markers were positioned at six loci in a map 24.1 centimorgans long. Six RAPD markers, including one identified in the F3MDH population, were mapped at the Rk locus.}, number={12}, journal={PLANT DISEASE}, author={Yi, HY and Rufty, RC and Wernsman, EA and Conkling, MC}, year={1998}, month={Dec}, pages={1319–1322} }
 @article{rufty_wernsman_main_gooding_1990, title={REGISTRATION OF NC-BMR 42 AND NC-BMR 90 GERMPLASM LINES OF TOBACCO}, volume={30}, ISSN={["0011-183X"]}, DOI={10.2135/cropsci1990.0011183X003000010071x}, abstractNote={Crop ScienceVolume 30, Issue 1 cropsci1990.0011183X003000010071x p. 241-242 Registration of Germplasms Registration of NC-BMR 42 and NC-BMR 90 Germplasm Lines of Tobacco R. C. Rufty, Corresponding Author R. C. Rufty n/[email protected] Dep. of Crop ScienceCorresponding author.Search for more papers by this authorE. A. Wernsman, E. A. Wernsman Dep. of Crop ScienceSearch for more papers by this authorC. E. Main, C. E. Main Dep. of Crop ScienceSearch for more papers by this authorG. V. Gooding Jr., G. V. Gooding Jr. Dep. of Plant Pathology, North Carolina State University, Raleigh, NC, 27695Search for more papers by this author R. C. Rufty, Corresponding Author R. C. Rufty n/[email protected] Dep. of Crop ScienceCorresponding author.Search for more papers by this authorE. A. Wernsman, E. A. Wernsman Dep. of Crop ScienceSearch for more papers by this authorC. E. Main, C. E. Main Dep. of Crop ScienceSearch for more papers by this authorG. V. Gooding Jr., G. V. Gooding Jr. Dep. of Plant Pathology, North Carolina State University, Raleigh, NC, 27695Search for more papers by this author First published: 01 January 1990 https://doi.org/10.2135/cropsci1990.0011183X003000010071xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume30, Issue1January–February 1990Pages 241-242 RelatedInformation}, number={1}, journal={CROP SCIENCE}, author={RUFTY, RC and WERNSMAN, EA and MAIN, CE and GOODING, GV}, year={1990}, pages={241–242} }
 @article{rufty_main_1989, title={COMPONENTS OF PARTIAL RESISTANCE TO BLUE MOLD IN 6 TOBACCO GENOTYPES UNDER CONTROLLED ENVIRONMENTAL-CONDITIONS}, volume={79}, ISSN={["0031-949X"]}, DOI={10.1094/Phyto-79-606}, abstractNote={Rufty, R. C., and Main, C. E. 1989. Components of partial resistance to blue mold in six tobacco genotypes under controlled environmental conditions. Phytopathology 79:606-609. Two susceptible and four partially resistant tobacco genotypes were Mutant, NC-BMR 42, and NC-BMR 90 produced fewer and smaller evaluated for components of partial resistance to blue mold. Disease lesions, had lower sporulation capacity, and exhibited longer patent efficiency, incubation period, latent period, degree of colonization, and periods than susceptible genotypes. Breeding line NC-BMR 90 was sporulation capacity were measured under high and low inoculation superior to all other partially resistant genotypes in this study. The presence density in experiments conducted at the Southeastern Plant Environmental of multiple resistance components in NC-BMR 90 makes this line a Laboratory (North Carolina State University Phytotron), Raleigh, NC. desirable source of blue mold resistance. Results obtained in these Genotypes differed significantly for all components of resistance in all experiments corroborated field observations and indicate that deployment trials. Commercial cultivars Speight G-70 and McNair 944 were of tobacco germ plasm with partial resistance to blue mold should reduce consistently the most susceptible genotypes based on all components of onset and progress of blue mold epidemics. partial resistance measured. Partially resistant genotypes Chemical Additional keywords: Nicotiana tabacum, Peronospora tabacina. Tobacco blue mold, also known as downy mildew of tobacco derived from N. velutina) and Chemical Mutant (resistance (Nicotiana tabacum L.), is caused by the fungus Peronospora obtained after treating seeds of flue-cured tobacco cultivar tabacina Adam. Occurrence of blue mold is generally sporadic, but Virginia Gold with triethylene iminotriazine) (9); two resistant severe economic losses can occur when the disease reaches breeding lines, NC-BMR 42 (derived from the cross Ovens 62 X epidemic proportions. For example, an epidemic of blue mold in McNair 944) and NC-BMR 90 (derived from the cross Ovens 62 X 1979 resulted in an estimated $250 million loss to U.S. and KY 17) (12); and two susceptible commercial cultivars, Speight}, number={5}, journal={PHYTOPATHOLOGY}, author={RUFTY, RC and MAIN, CE}, year={1989}, month={May}, pages={606–609} }
 @inbook{rufty_1989, title={Genetics of host resistance to tobacco blue mold}, ISBN={0890540977}, booktitle={Blue mold of tobacco}, publisher={St. Paul, Minn.: APS Press}, author={Rufty, R. C.}, year={1989}, pages={141} }